CAMHS & Eating Disorders Flashcards

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1
Q

What is the 4P factor model in regards to child psychology?

A

Predisposing
Precipitating
Perpetuating
Protective

Takes a biopsychosocial approach

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2
Q

What types of ADHD are there?

A

Predominately inattentive (20-30%), predominately hyperactive-impulsive (15%) or combined type (50-75%)

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3
Q

How is ADHD diagnosed?

A

> 6 months inattention and/or hyperactivitity-impulsivity

Negative impact on academic, occupational or social functioning

Symptoms present in more than 1 setting i.e. home AND school

Not better explained by another disorder e.g. Autism, anxiety, FASD, ODD
Prevalence around 5% in children

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4
Q

In who does ADHD typically present?

A

Symptoms usually evident before age 12

M:F 3:1

Hyperactive-impulsive symptoms tend to recede, inattentive symptoms may persist

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5
Q

How is ADHD assessed?

A

Focused history, psychometrics e.g. Conners, school report, school obs to assess

ADHD focused group parent-training programme e.g. PINC is 1st line

Consider if school adjustments needed
Assess for comorbidities e.g. ASD, OCD, ODD, conduct disorder, anxiety

  • 1 instruction at a time
  • Brain breaks
  • Don’t restrict fidgeting if not detrimental
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6
Q

What medication can be used for ADHD?

A

If medication required, must monitor height, weight, BP, HR, check for personal or family history of sudden cardiac events or breathlessness/fatigue/syncope on exertion

1) Methylphenidate 1st line (immediate or prolonged release)

2) Lisdexamphetamine 2nd line

3) Atomoxetine or guanfacine 3rd line (non-stimulants)

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7
Q

What triad of symptoms is present in autism spectrum disorder?

A

Impairments in reciprocal social interactions

Difficulties with social communication

Restricted, repetitive and inflexible patterns of interest or behaviour

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8
Q

When does onset of Autism spectrum disorder typically present and how?

A

Onset usually during early childhood, but may not become apparent until later

Deficits cause impairment in functioning

Evident across settings

Individuals may or may not have disorders of intellectual development or impaired functional language

Prevalence 1-2% of children, M:F approx. 4:1

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9
Q

How is autism spectrum disorder assessed and managed?

A

Higher incidence of sleep disorders, ADHD, anxiety, depression OCD and tics

Developmental history is cornerstone, can use structured interview e.g. ADI-R or 3Di, MDT assessment ideal to assess strengths and weaknesses

If further assessment required – ADOS, school reports and questionnaires, school observation

Parent-mediated intervention programme offered to all e.g. Cygnet

Behavioural interventions or environmental adjustments

Support for communication e.g. PECS, visual supports

Melatonin for sleep disorders, Aripiprazole or Risperidone for irritability or aggression

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10
Q

How are anxiety disorders assessed and managed?

A

Clinical history and examination, parent and school report

Can use psychometrics such as RCADS, C-YBOCS

Psychoeducation (directed to child or parent as appropriate)

Schools based intervention frequently

CBT, Graded exposure, Exposure response prevention, SLT, OT, Physio as appropriate

SSRI can be considered if inadequate response

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11
Q

Conduct disorders such as oppositional defiant disorder and conduct dissocial disorder are the most common mental & behavioural disorder in children: How do they present?

A

Increased risk in:
- Lower social classes
- LAAC
- Children who have been abused
- Children on the child protection register

> 6 months duration

ODD commoner in those age 10 and under, CD usually in those 11 and over

M>F

Significant comorbidity with ADHD

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12
Q

50% of those with conduct disorder go on to develop Antisocial PD: What is this associated with?

A

Associated with later:
- Poor educational attainment
- Social isolation
- Substance misuse
- Criminality

Assessed through clinical history from parents, observation of child, school report, psychometrics

Management – parenting programmes and multisystemic approaches via Social Work

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13
Q

How does ODD present compared to CD?

A

ODD:
- Markedly defiant, disobedient, provocative or spiteful behaviour
- Persistent angry/irritable mood, severe temper outbursts
- Argumentative/defiant behaviour
- Causes significant impairment in functioning

CD:
- Persistent violation of basic rights of others or major societal norms
- Aggression towards people, animals or property
- Deceitfulness, theft
- Serious violation of rules or laws
- Significant impairment in functioning

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14
Q

What is included in a MSE?

A

A= Appearance and behavior
S= Speech
E= Emotions (objective & subjective)
P= Perceptions
T= Thoughts (thought form and thought content)
I= Insight
C= Cognition

Risk – deteriation in ms, risks of neglect, vulnerability etc

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15
Q

What are risk factors for acute psychosis?

A
  • Presents in late adolescence-early adulthood
  • M>F
  • Positive family history of psychotic illness common

Risk of developing psychosis is higher:
- ID and ASD population
- Urban environment, low SES, migrant or refugee
- Childhood adversity
- ?all are exposure to chronic social stress

  • An acute stressor, poor sleep and illicit drug use can sometimes be identified as the acute trigger
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16
Q

How does acute psychosis typically present?

A

Initially social withdrawal, unusual or over-valued ideas or paranoia, heightened anxiety = prodromal phase

May progress to full blown acute psychosis with hallucinations and delusions

Usually with self neglect, a lack of insight and significant vulnerability

17
Q

How is acute psychosis investigated?

A

Full neurology exam

Observations

Bloods including anti-NMDA receptor Abs

Urine drug screen

CT or MRI head

18
Q

How is acute psychosis managed?

A

Treat any organic cause eg. Brain tumour, NMDAR encephalitis, drug-induced psychosis (steroids, retinoids)

Consider if inpatient admission required

Start antipsychotic – aripiprazole first choice in adolescence
- Low threshold for adding antidepressant

New ICD-11 recommendation to describe features of psychosis rather than try to fit into category eg. Bipolar or schizophrenia
Don’t jump to diagnosis – this can take around 2 years

19
Q

What antipsychotic is the first choice in adolescence?

A

Aripiprazole

20
Q

What are risk factors for BPD?

A
  • Presents at puberty
  • F>M
  • Childhood adversity
  • Spectrum from invalidating environment - abuse
  • Genetic – temperament, impulsivity
  • Family history of BPD, alcohol misuse
  • Neurodevelopmental disorder
21
Q

How does BPD present typically?

A

Usual presentation to CAMHS is self harm and low mood

Suicidal behaviours – acute presentation post-overdose

Increasingly chaotic relationships

Alcohol and drug misuse

At severe end – paranoia, hearing voices and dissociation

22
Q

How is BPD investigated and managed?

A

Investigations:
Thorough psychiatric assessment

Management:
- Ensure safety – parental supervision, whilst assessing
- Crisis plan
- Crux of treatment is understanding BPD, then learning to manage emotional instability and learn new coping skills
- Key is validating and consistent therapeutic relationship
- Management is in the community, inpatient admission can be very damaging
- Social work or third sector involvement is often required

23
Q

Are medications used in BPD?

A

Medications are not generally helpful

24
Q

What is anorexia nervosa diagnosed by?

A

Significantly low body weight for height. BMI <18.5, (<5th centile in children), rapid weight loss >20% in 6 months.

Relies on compulsive compensatory behaviours when food cannot be avoided, Self induced vomiting, laxative abuse, excessive exercise, abuse of appetite suppressants / diuretics.

25
Q

What are the signs & symptoms of anorexia nervosa?

A

Cold intolerance, Blue hands and feet
Constipation, Bloating
Delayed puberty
Primary or secondary amenorrhea
Dry skin
Fainting, Hypotension
Lanugo hair, Scalp hair loss
Early satiety
Weakness, fatigue
Short stature
Osteopenia & osteoporosis

  • Loss of muscle
  • Heart rate slows as a protective mechanism of the heart muscle
  • Only treatment is vitamins-not pharmacological
26
Q

How is bulimia nervosa defined?

A

Binges and the resulting compensatory behaviour must occur a minimum of once per week over at least a month.

  • Episodes of binge eating with a sense of loss of control
  • Binge eating is followed by compensatory behaviour of the purging type (self-induced vomiting, laxative abuse, diuretic abuse, insulin omission) or nonpurging type (excessive exercise, fasting, or strict diets).
27
Q

What are some signs & symptoms of bulimia nervosa?

A

Mouth sores, Pharyngeal trauma, Dental caries, Esophageal rupture

Heartburn, chest pain

Impulsivity:
Stealing
Alcohol abuse
Drugs/tobacco

Muscle cramps

Weakness

Bloody diarrhoea

Irregular periods

Fainting

Swollen parotid glands

Hypotension

28
Q

How can cardiac issues be associated with Bulimia nervosa?

A

Issues with potassium-cardiac issues –with so much induced vomiting

29
Q

What is a binge eating disorder?

A

Similar to bulimia nervosa; absence of purging behaviours.

Ongoing and/or repetitive cycles often include:
- unusually fast eating, usually alone.
- unusually large amounts consumed.
- uncomfortably full; often “buzzed” after eating.
- embarrassment, shame, guilt, depression.

30
Q

What is TIDE?

A

Eating disorders in Type 1 Diabetes

  • Food restriction – anorexia variant
  • Binging- bulimic variant

Under use of insulin

31
Q

What is Other specified feeding or eating disorder (OSFED)?

A

A person may have OSFED if their symptoms do not exactly fit the expected symptoms for any specific ED. Some examples are Atypical anorexia ( similar behaviours but weight remains within a normal range) or Atypical bulimia ( binges don’t happen as often or over as long a period of time). Purging disorder, not part of a binge/purge cycle. Night eating syndrome.

This is the most common eating disorder.

32
Q

What is Avoidant Restrictive Food intake disorder. ( ARFID)?

A

Avoidance or restriction of food intake for a number of reasons.

Eg, sensitivity to texture, smell or appearance of certain foods. A previous bad experience with food EG choking or vomiting leading to concern about the consequences of eating.

It may result in weight loss and nutrition and psychological deficits.

The behaviours are NOT motivated by a pre-occupation of weight and shape.

33
Q

What are the causes of anorexia?

A

Genetic predisposition – OCD, anxiety disorders, perfectionism, low self-esteem

Perinatal factors

Life events – and traumas

Perpetuating consequences of starvation and of avoidance

34
Q

What are the precipitating factors in EDs?

A

Puberty – physical effects of hormonal changes on the brain , also psychological response to body changes

Dieting or even non-deliberate weight loss

Increased exercise

Stressful life events

35
Q

What are the perpetuating factors in anorexia?

A

Consequences of ‘starvation syndrome’

  • Delayed gastric emptying - sensations of fullness interpreted as fatness,
  • Narrowing focus with avoidance of interpersonal interest, change of values so that food becomes the most salient stimulus
  • Obsessionality. Phobia of ‘fat’ increases as avoidance increases. ‘Body checking’ amplifies body image concern
  • Families, School, Clinic staff
    High EE in family (and other carers) may delay recovery
36
Q

What is the average time for recovery from anorexia nervosa?

A

Average time for recovery from anorexia nervosa – where this occurs – has been estimated at 6 – 7 years.

Specialist centres report some recoveries after decades.

37
Q

How can AN be helped?

A
  • Re-feeding
  • CBT –ED, ( 40 sessions)Mantra (20 sessions) SSCM( 20 sessions) CBT(including self-help) for normal weight Bulimia Nervosa
  • Alternatively IPT, or fluoxetine 60mg daily (in fact any antidepressant in high dose)
  • Olanzapine
  • Specialised family work for anorexia nervosa, particularly for younger patients